title: Relation of coronary microvascular dysfunction in hypertrophic cardiomyopathy to contractile dysfunction independent from myocardial injury.
abstract: We studied the spatial relations among hyperemic myocardial blood flow (hMBF), contractile function, and morphologic tissue alterations in 19 patients with hypertrophic cardiomyopathy (HC). All patients were studied with oxygen-15 water positron emission tomography during rest and adenosine administration to assess myocardial perfusion. Cardiovascular magnetic resonance was performed to derive delayed contrast-enhanced images and to calculate contractile function (E(cc)) with tissue tagging. Eleven healthy subjects underwent similar positron emission tomographic and cardiovascular magnetic resonance scanning protocols and served as a control group. In the HC group, hMBF averaged 2.46 ± 0.91 ml/min/g and mean E(cc) was -14.7 ± 3.4%, which were decreased compared to the control group (3.97 ± 1.48 ml/min/g and -17.7 ± 3.2%, respectively, p <0.001 for the 2 comparisons). Delayed contrast enhancement (DCE) was present only in patients with HC, averaging 6.2 ± 10.3% of left ventricular mass. In the HC group, E(cc) and DCE in the septum (-13.7 ± 3.6% and 10.2 ± 13.6%) significantly differed from the lateral wall (-16.0 ± 2.8% and 2.4 ± 5.9%, p <0.001 for the 2 comparisons). In general, hMBF and E(cc) were decreased in segments displaying DCE compared to nonenhanced segments (p <0.001 for the comparisons). In the HC group, univariate analysis revealed relations of hMBF to E(cc) (r = -0.45, p <0.001) and DCE (r = -0.31, p <0.001). Multivariate analysis revealed that E(cc) was independently related to hMBF (beta -0.37, p <0.001) and DCE (beta 0.28, p <0.001). In conclusion, in HC hMBF is impaired and related to contractile function independent from presence of DCE. When present, DCE reflected a progressed disease state as characterized by an increased perfusion deficit and contractile dysfunction.
authors.affiliation: Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands.
authors.forename: Stefan A J
authors.initials: SA
authors.lastname: Timmer
authors.forename: Tjeerd
authors.initials: T
authors.lastname: Germans
authors.forename: Marco J W
authors.initials: MJ
authors.lastname: Götte
authors.forename: Iris K
authors.initials: IK
authors.lastname: Rüssel
authors.forename: Mark
authors.initials: M
authors.lastname: Lubberink
authors.forename: Jurrien M
authors.initials: JM
authors.lastname: Ten Berg
authors.forename: Folkert J
authors.initials: FJ
authors.lastname: Ten Cate
authors.forename: Adriaan A
authors.initials: AA
authors.lastname: Lammertsma
authors.forename: Paul
authors.initials: P
authors.lastname: Knaapen
authors.forename: Albert C
authors.initials: AC
authors.lastname: van Rossum
mesh_terms: D002312:Cardiomyopathy, Hypertrophic / Q000503:physiopathology*; D002319:Cardiovascular System; D003326:Coronary Circulation / Q000502:physiology*; D003331:Coronary Vessels / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D055806:Microvessels / Q000503:physiopathology*; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology; D049268:Positron-Emission Tomography